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Sökning: WFRF:(Landén Mikael 1966 ) > Naturvetenskap

  • Resultat 1-4 av 4
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1.
  • Karanti, Alina (Aikaterini), et al. (författare)
  • Gender differences in the treatment of patients with bipolar disorder: A study of 7354 patients
  • 2015
  • Ingår i: Journal of Affective Disorders. - : Elsevier BV. - 0165-0327 .- 1573-2517. ; 174, s. 303-309
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Gender differences in treatment that are not supported by empirical evidence have been reported in several areas of medicine. Here, the aim was to evaluate potential gender differences in the treatment for bipolar disorder. Methods: Data was collected from the Swedish National Quality Assurance Register for bipolar disorder (BipolaR). Baseline registrations from the period 2004-2011 of 7354 patients were analyzed. Multiple logistic regression analysis was used to study the impact of gender on interventions. Results: Women were more often treated with antidepressants, lamotrigine, electroconvulsive therapy, benzodiazepines, and psychotherapy. Men were more often treated with lithium. There were no gender differences in treatment with mood stabilizers as a group, neuroleptics, or valproate. Subgroup analyses revealed that ECT was more common in women only in the bipolar l subgroup. Contrariwise, lamotrigine was more common in women only in the bipolar II subgroup. Limitations: As BipolaR contains data on outpatient treatment of persons with bipolar disorder in Sweden, it is unclear if these Findings translate to inpatient care and to outpatient treatment in other countries. Conclusions: Men and women with bipolar disorder receive different treatments in routine clinical settings in Sweden. Gender differences in level of functioning, bipolar subtype, or severity of bipolar disorder could not explain the higher prevalence of pharmacological treatment, electroconvulsive therapy, and psychotherapy in women. Our results suggest that clinicians' treatment decisions are to some extent unduly influenced by patients' gender. (C) 2014 Elsevier B.V. All rights reserved.
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2.
  • Chang, H., et al. (författare)
  • The protocadherin 17 gene affects cognition, personality, amygdala structure and function, synapse development and risk of major mood disorders
  • 2018
  • Ingår i: Molecular Psychiatry. - : Springer Science and Business Media LLC. - 1359-4184 .- 1476-5578. ; 23:2, s. 400-412
  • Tidskriftsartikel (refereegranskat)abstract
    • Major mood disorders, which primarily include bipolar disorder and major depressive disorder, are the leading cause of disability worldwide and pose a major challenge in identifying robust risk genes. Here, we present data from independent large-scale clinical data sets (including 29 557 cases and 32 056 controls) revealing brain expressed protocadherin 17 (PCDH17) as a susceptibility gene for major mood disorders. Single-nucleotide polymorphisms (SNPs) spanning the PCDH17 region are significantly associated with major mood disorders; subjects carrying the risk allele showed impaired cognitive abilities, increased vulnerable personality features, decreased amygdala volume and altered amygdala function as compared with non-carriers. The risk allele predicted higher transcriptional levels of PCDH17 mRNA in postmortem brain samples, which is consistent with increased gene expression in patients with bipolar disorder compared with healthy subjects. Further, overexpression of PCDH17 in primary cortical neurons revealed significantly decreased spine density and abnormal dendritic morphology compared with control groups, which again is consistent with the clinical observations of reduced numbers of dendritic spines in the brains of patients with major mood disorders. Given that synaptic spines are dynamic structures which regulate neuronal plasticity and have crucial roles in myriad brain functions, this study reveals a potential underlying biological mechanism of a novel risk gene for major mood disorders involved in synaptic function and related intermediate phenotypes.
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3.
  • Isgren, Anniella, et al. (författare)
  • Cerebrospinal fluid proteomic study of two bipolar disorder cohorts
  • 2022
  • Ingår i: Molecular Psychiatry. - : Springer Science and Business Media LLC. - 1359-4184 .- 1476-5578. ; 27:11, s. 4568-4574
  • Tidskriftsartikel (refereegranskat)abstract
    • The pathophysiology of bipolar disorder remains to be elucidated and there are no diagnostic or prognostic biomarkers for the condition. In this explorative proteomic study, we analyzed 201 proteins in cerebrospinal fluid (CSF) from mood stable bipolar disorder patients and control subjects sampled from two independent cohorts, amounting to a total of 204 patients and 144 controls. We used three Olink Multiplex panels, whereof one specifically targets immune biomarkers, to assess a broad set of CSF protein concentrations. After quality control and removal of proteins with a low detection rate, 105 proteins remained for analyses in relation to case-control status and clinical variables. Only case-control differences that replicated across cohorts were considered. Results adjusted for potential confounders showed that CSF concentrations of growth hormone were lower in bipolar disorder compared with controls in both cohorts. The effect size was larger when the analysis was restricted to bipolar disorder type 1 and controls. We found no indications of immune activation or other aberrations. Growth hormone exerts many effects in the central nervous system and our findings suggest that growth hormone might be implicated in the pathophysiology of bipolar disorder.
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4.
  • Munn-Chernoff, M. A., et al. (författare)
  • Shared genetic risk between eating disorder- and substance-use-related phenotypes: Evidence from genome-wide association studies
  • 2021
  • Ingår i: Addiction Biology. - : Wiley. - 1355-6215 .- 1369-1600. ; 26:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Eating disorders and substance use disorders frequently co-occur. Twin studies reveal shared genetic variance between liabilities to eating disorders and substance use, with the strongest associations between symptoms of bulimia nervosa and problem alcohol use (genetic correlation [r(g)], twin-based = 0.23-0.53). We estimated the genetic correlation between eating disorder and substance use and disorder phenotypes using data from genome-wide association studies (GWAS). Four eating disorder phenotypes (anorexia nervosa [AN], AN with binge eating, AN without binge eating, and a bulimia nervosa factor score), and eight substance-use-related phenotypes (drinks per week, alcohol use disorder [AUD], smoking initiation, current smoking, cigarettes per day, nicotine dependence, cannabis initiation, and cannabis use disorder) from eight studies were included. Significant genetic correlations were adjusted for variants associated with major depressive disorder and schizophrenia. Total study sample sizes per phenotype ranged from similar to 2400 to similar to 537 000 individuals. We used linkage disequilibrium score regression to calculate single nucleotide polymorphism-based genetic correlations between eating disorder- and substance-use-related phenotypes. Significant positive genetic associations emerged between AUD and AN (r(g) = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN (r(g) = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating (r(g) = 0.27; q = 0.0016). Conversely, significant negative genetic correlations were observed between three nondiagnostic smoking phenotypes (smoking initiation, current smoking, and cigarettes per day) and AN without binge eating (r(gs) = -0.19 to -0.23; qs < 0.04). The genetic correlation between AUD and AN was no longer significant after co-varying for major depressive disorder loci. The patterns of association between eating disorder- and substance-use-related phenotypes highlights the potentially complex and substance-specific relationships among these behaviors.
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